Evidence map›Paper›PMID 29776428›Full record

ArticleJournal of neuroinflammation2018

Evidence of the impact of systemic inflammation on neuroinflammation from a non-bacterial endotoxin animal model.

Chunxia Huang, Michael Garnet Irwin, Gordon Tin Chun Wong, Raymond Chuen Chung Chang

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
4.6field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

68 citing papers in PubMed, 121 citations in OpenAlex.

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  11. Ultrasound-Assisted HAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  12. Review
  13. Pentoxifylline Prevents Neuroinflammation and Modifies PTEN/TrkB Signaling in an LPS-Induced Depression Model.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025
    Article
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8 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Chunxia HuangDepartment of Anaesthesiology, LKS Faculty of Medicine, The University of Hong Kong, Room K424, Queen Mary Hospital, Pokfulam, Hong Kong SAR, China.
Michael Garnet IrwinDepartment of Anaesthesiology, LKS Faculty of Medicine, The University of Hong Kong, Room K424, Queen Mary Hospital, Pokfulam, Hong Kong SAR, China.
Gordon Tin Chun WongDepartment of Anaesthesiology, LKS Faculty of Medicine, The University of Hong Kong, Room K424, Queen Mary Hospital, Pokfulam, Hong Kong SAR, China. gordon@hku.hk.
Raymond Chuen Chung ChangLaboratory of Neurodegenerative Diseases, School of Biomedical Sciences, LKS Faculty of Medicine, The University of Hong Kong, Room L4-49, Laboratory Block, Faculty of Medicine Building, 21 Sassoon Road, Pokfulam, Hong Kong SAR, China. rccchang@hku.hk.
Queen Mary Hospital · CNUniversity of Hong Kong · HK

Funding

General Research Fund, Research Grant Council, Hong Kong 17123217HKU Seed Funding Program for Basic Research 201311159069 and 201411159086
6 · The paper itself

Abstract

backgroundSystemic inflammation induces neuroinflammation and cellular changes such as tau phosphorylation to impair cognitive function, including learning and memory. This study uses a single model, laparotomy without any pathogen, to characterize these changes and their responses to anti-inflammatory treatment in the intermediate term.

methodsIn a two-part experiment, wild-type C57BL/6N mice (male, 3 month old, 25 ± 2 g) were subjected to sevoflurane anesthesia alone or to a laparotomy. Cognitive performance, systemic and neuroinflammatory responses, and tau phosphorylation were evaluated on postoperative days (POD) 1, 3, and 14. The effect of perioperative ibuprofen intervention (60 mg/kg) on these changes was then assessed.

resultsMice in the laparotomy group displayed memory impairment up to POD 14 with initial high levels of inflammatory cytokines in the liver, frontal cortex (IL-1β, IL-6, and TNF-α), and hippocampus (IL-1β and IL-8). On POD 14, although most circulating and resident cytokine levels returned to normal, a significant number of microglia and astrocytes remained activated in the frontal cortex and microglia in the hippocampus, as well as abnormal tau phosphorylation in these two brain regions. Perioperative ibuprofen improved cognitive performance, attenuated systemic inflammation and glial activation, and suppressed the abnormal tau phosphorylation both in the frontal cortex and hippocampus.

conclusionsOur results suggest that (1) cognitive dysfunction is associated with an unbalanced pro-inflammatory and anti-inflammatory response, tauopathy, and gliosis; (2) cognitive dysfunction, gliosis, and tauopathy following laparotomy can persist well beyond the immediate postoperative period; and (3) anti-inflammatory drugs can act rapidly to attenuate inflammatory responses in the brain and negatively modulate neuropathological changes to improve cognition. These findings may have implications for the duration of therapeutic strategies aimed at curtaining cognitive dysfunction following surgery.

Indexed as

Anesthetics, InhalationAnimalsBody WeightBrainCalcium-Binding ProteinsCytokinesDisease Models, AnimalEncephalitisExploratory BehaviorGene Expression RegulationLaparotomyLiverMaleMaze LearningMemory DisordersMiceAif1 protein, mouseAnesthetics, InhalationCalcium-Binding ProteinsCytokinesMicrofilament ProteinsSevofluranetau ProteinsIbuprofenNeuroinflammationPostoperative cognitive dysfunctionSevofluraneTau proteins

Identifiers

PMID29776428
PMCPMC5960121
OpenAlexW2805858230

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.